کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2202647 | 1551394 | 2014 | 6 صفحه PDF | دانلود رایگان |
• Aneuploidy is deleterious at the cellular and organismal level.
• Aneuploidy induces JNK-dependent apoptosis in epithelial cells.
• Aneuploidy drives JNK-dependent tumorigenesis upon apoptosis blockade.
• A stress-induced tumor-promoting activity of aneuploidy is proposed.
Aneuploidy, described as an abnormal number of whole chromosomes or parts of them, has been observed in the majority of sporadic carcinomas, the most common type of cancer occurring in humans and derived from putative epithelial cells. However, the causal relationship between aneuploidy and tumorigenesis remains highly debated. On the one hand, aneuploidy has been shown to be a powerful driver of tumor progression, anticancer drug resistance, and tumor relapse. On the other hand, aneuploidy causes proteotoxic and metabolic stress, which compromises cell cycle proliferation and growth. Here we discuss the role of aneuploidy in tumorigenesis in light of the contribution of Drosophila epithelial cancer models and propose a stress-induced tumor-promoting role of aneuploidy.
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Journal: Seminars in Cell & Developmental Biology - Volume 28, April 2014, Pages 110–115